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Differential gene expression profiles between two novel murine prostate cancer cell lines derived from androgen‑dependent (PLum‑AD cells) and androgen‑independent (PLum‑AI cells) prostate cancer

ABSTRACT: Orthotopic tumors were previously generated from parental Prostate Luminal (PLum) cells under androgen‑dependent (PLum-AD) and androgen‑independent (PLum-AI) conditions in order to establish cellular models of prostate cancer progression (Abou-Kheir et al., 2011; doi: 10.1371/journal.pone.0026112). We used microarrays to evaluate the differential gene expression profiles underlying progression of prostate cancer from primary androgen-dependent stage to advanced androgen-independent stage using newly isolated murine prostate cancer cell lines. Those cell lines represent novel in vitro models of androgen‑dependent and –independent prostate cancer, recapitulating the progression of the disease to a more invasive phenotype upon androgen deprivation.

ORGANISM(S): Mus musculus

PROVIDER: GSE151187 | GEO | 2020/05/27

REPOSITORIES: GEO

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Project description:Following androgen ablation therapy (AAT), the vast majority of prostate cancer patients develop treatment resistance with a median time of 18-24 months to disease progression. To identify molecular targets that aid in prostate cancer cell survival and contribute to the androgen independent phenotype, we evaluated changes in LNCaP cell gene expression during 12 months of androgen deprivation. At time points reflecting critical growth and phenotypic changes, we performed Affymetrix expression array analysis to examine the effects of androgen deprivation during the acute response, during the period of apparent quiescence, and during the emergence of highly proliferative, androgen-independent prostate cancer cells (LNCaP-AI). We discovered alterations in gene expression for a host of molecules associated with promoting prostate cancer cell growth and survival, regulating cell cycle progression, apoptosis and adrenal androgen metabolism, in addition to AR co-regulators and markers of neuroendocrine disease. These findings illustrate the complexity and unpredictable nature of cancer cell biology and contribute greatly to our understanding of how prostate cancer cells likely survive AAT. The value of this longitudinal approach lies in the ability to examine gene expression changes throughout the cellular response to androgen deprivation; it provides a more dynamic illustration of those genes which contribute to disease progression in addition to specific genes which constitute a malignant androgen-independent phenotype. In conclusion, it is of great importance that we employ new approaches, such as the one proposed here, to continue exploring the cellular mechanisms of therapy resistance and identify promising targets to improve cancer therapeutics. Experiment Overall Design: To identify molecular targets that aid in prostate cancer cell survival and contribute to the androgen independent phenotype, we evaluated changes in LNCaP cell gene expression during 12 months of androgen deprivation. At time points reflecting critical growth and phenotypic changes, we performed Affymetrix expression array analysis to examine the effects of androgen deprivation during the acute response, during the period of apparent quiescence, and during the emergence of highly proliferative, androgen-independent prostate cancer cells (LNCaP-AI).

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Differential gene expression profiles between two novel murine prostate cancer cell lines derived from androgen‑dependent (PLum‑AD cells) and androgen‑independent (PLum‑AI cells) prostate cancer

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